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Plasma ghrelin concentrations in elderly subjects: comparison with anorexic and obese patients.
TLDR
Evidence of an age-related decline of plasma ghrelin concentrations is provided, which might explain, at least partially, the somatotroph dysregulation and the anorexia of the elderly subject.
Metronomic combination of Vinorelbine and 5Fluorouracil is able to inhibit triple-negative breast cancer cells. Results from the proof-of-concept VICTOR-0 study
TLDR
Molecular mechanisms implicated in apoptosis and autophagy as well as the cross-talk between these two forms of cell death in MDA-MB-231 and BT-549 cells treated with 5FU and VNR is dose- and schedule-dependent and some insights about the roles of Autophagy and senescence in 5FU/VNR-induced cell death are provided.
Effect of somatostatin infusion on peptide YY secretion: studies in the acute and recovery phase of anorexia nervosa and in obesity.
TLDR
The results suggest the existence of a hypo- and hyper-sensitivity of L cells to the inhibitory effect of SRIF in A-AN and OB respectively.
p65BTK is a novel potential actionable target in KRAS-mutated/EGFR-wild type lung adenocarcinoma
TLDR
Adding BTK-TKIs to SOC chemotherapy and EGFR-targeted therapy may open new avenues for clinical trials in currently untreatable NSCLC, as p65BTK results as an emerging actionable target in non-smoking EGfr-wt AdC, also at advanced stages of disease.
Growth hormone (GH) rebound rise following somatostatin infusion withdrawal: studies in dogs with the use of GH-releasing hormone and a GH-releasing peptide.
TLDR
The uniformity of the GH rebound responses to multiple cycles of SSIW may indicate that the latter activate a physiological mechanism which mimics that normally controlling GH pulse generation.
GSK3A Is Redundant with GSK3B in Modulating Drug Resistance and Chemotherapy-Induced Necroptosis
TLDR
GSK3A is redundant with GSK3B in regulating drug-resistance and chemotherapy-induced necroptosis and it is suggested that inhibition of only one isoform, or rather partial inhibition of overall cellular G SK3 activity, is enough to re-sensitize drug-resistant cells to chemotherapy.
BTK inhibitors synergise with 5‐FU to treat drug‐resistant TP53‐null colon cancers
TLDR
It is demonstrated that targeting p65BTK restores the apoptotic response to chemotherapy of drug‐resistant CRCs and gives a proof‐of‐concept for suggesting the use of BTK inhibitors in combination with 5‐FU as a novel therapeutic approach in CRC patients.
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